Pandemic Influenza A (H1N1) Outbreak in 15 School-Aged HIV-Infected Children
Background For patients infected with the human immunodeficiency virus type 1 (HIV-1), the clinical course and overall health risk after 2009 H1N1 influenza virus infection is not well established. Objective Describe the clinical course, kinetics of viral shedding, and the H1N1 influenza-specific humoral immune response among HIV-infected children. Methods Observational study after an outbreak of 2009 H1N1 influenza virus infections among a travel group of 15 HIV-infected children (aged 8.9–16.8 years) in Germany in October 2009. All children had been treated with highly active antiretroviral therapy and had CD4 cell counts exceeding 350/µL. Disease symptoms were recorded and shedding of H1N1 influenza virus was assessed by detection of virus-specific RNA and culture of virus from nasal secretions. Serum levels of H1N1-specific antibodies were determined at 6 weeks after symptom-onset. Results In all 15 children of the travel group, infection with the 2009 H1N1 influenza virus was confirmed by viral culture and reverse transcriptase polymerase chain reaction from nasal secretions (n=11) and/or detection of 2009 H1N1-specific antibodies. Fourteen children (93%) had symptoms of disease, mostly consisting of low-grade fevers and cough. Five children (33%) had high-grade fevers (>39°C) and, thus, were treated with oseltamivir. Among the 11 children in whom viral shedding was assessed, viral RNA was detected for 4 versus 8 days (p=0.005), and cell cultures tested positive for 3 versus 6 days (p=0.005), respectively, among oseltamivir-treated (n=5) and non-treated (n=6) children. At 6 weeks after symptoms-onset, all children had developed H1N1 virus-specific antibodies. Conclusions Clinical course, kinetics of viral shedding, and rate of emergence of virus-specific antibodies among school-aged HIV-infected children with 2009 H1N1 influenza virus co-infection did not appear to be different from those described for healthy children. Oseltamivir shortens the duration of H1N1 influenza virus shedding in HIV-infected children.